1. Field of the Invention
The present invention relates generally to the field of oncology. More particularly, it concerns the detection of arginine methylation of EGFR to predict resistance to cetuximab therapy and sensitivity to a combination therapy using a PRMT inhibitor plus cetuximab.
2. Description of Related Art
Epidermal growth factor receptor (EGFR)-targeted monoclonal antibody, cetuximab, is one of the most effective ways of controlling colorectal cancer progression (Berg and Soreide, 2012). However, resistance to cetuximab has been observed in the clinic (Custodio and Feliu, 2013; Fabian and Berkovcova, 2011; Messner et al., 2013). Currently, the most accepted predictive marker for poor cetuximab response in colorectal cancer is mutant KRAS status due its association with poor patient survival rate (De Roock et al., 2008; Lievre et al., 2008). Nevertheless, studies show increasing evidence that wild-type KRAS is insufficient to confer sensitivity to cetuximab (Fabian and Berkovcova, 2011; Laurent-Puig et al., 2009; Silvestris et al., 2009) and that patients with mutant KRAS are not necessarily refractory to cetuximab (Custodio and Feliu, 2013; Messner et al., 2013; Mao et al., 2013; Tejpar et al., 2013; De Roock et al., 2010). Therefore, other predictors of cetuximab response are needed.